After reminding the epidemiology of the HTLV1 infection the authors sum up the actually recommended diagnosis procedure. --Case finding by ELISA, confirmation by WESTERN-BLOT and/or RIPA (anti-gag and anti-env specificities), or even PCR which makes specific diagnosis of HTLV1/2. --Or if possible directly by PCR which has helped some authors to find provirus in seronegative people. Coinfections caused by HIV and by Strongyloides are the best documented. As a rule, HTLV1 seems to have rather a worsening effect on evolutiveness and on seriousness of the clinical picture caused by mixed infections, than the contrary (possibly for lack of experience and owing to slow evolution of HTLV1 pathology). Several mechanisms have been proposed concerning coinfections with HTLV1 and HIV (in vitro studies). --Immortalization of CD4 lymphocytes infected with HTLV1 by stimulating both IL2 and its receptor, and by activating lymphocytes with translocation of the replicating factor NF k B in the nucleus, on a promoting sequence of HIV-LTR by stimulating its replication. --The product of HTLV1 tax gene would also have a transactivating effect on the provirus HIV-LTR replication. And finally infection with HTLV1 may facilitate HIV by inducing CD4, molecule expression in non-expressing cells. In Strongyloides modulating effects of HTLV1 on the immune response would facilitate and predispose Strongyloides stercoralis multiplication. As far as other coinfections are concerned (caused by viruses, by parasites: such as malaria, filariasis, trypanosomiasis or by bacteria), epidemiological convergence (risk factors, and geographic distribution) on the one hand, and immunological dysregulation induced by the other, on the other hand, would be of varying importance. In conclusion, these data ask more questions than they answer. But it seems to be established that detection of HIV and Strongyloides should performed in every case HTLV1 carries and vice versa.